Surprisingly, and in contrast to previous models where PHD2 was deleted from ECs starting from embryogenesis, Phd2∆ECi resulted in an increased pulmonary artery pressure gradient and cardiac hypertrophy without structural remodeling of the pulmonary arteries (i.e. no alterations in aSMC proliferation, arterial wall or periarterial extracellular matrix). The gene discussed is EGLN1; the disease is cardiac hypertrophy.